In:
Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 4 ( 1998-04), p. 1030-1034
Abstract:
Abstract —Possible impairment of the l -arginine–nitric oxide (NO) pathway in the rostral ventrolateral medulla of adult spontaneously hypertensive rats (SHR) was investigated by microinjecting N G -nitro- l -arginine methyl ester (L-NAME), NOC 18 (an NO donor), or l -arginine. Unilateral injection of L-NAME (10 nmol/50 nL) into the rostral ventrolateral medulla significantly increased mean arterial pressure (MAP) in both SHR and Wistar-Kyoto rats (WKY). The increases in MAP did not differ significantly between the two strains (15±3 versus 10±2 mm Hg, respectively; n=8). In contrast, microinjection of l- arginine elicited significant ( P 〈 .05) dose-dependent decreases in MAP in both strains, and these depressor responses were significantly greater in SHR than in WKY (in 10 nmol of l- arginine: –29±2 versus –15±2 mm Hg, respectively; n=8, P 〈 .01). Similarly, microinjection of NOC 18 (10 nmol/50 nL) reduced MAP in both strains, and the depressor response was also significantly greater in SHR than in WKY (–38±7 versus –22±3 mm Hg, respectively; n=8, P 〈 .05). These results suggest that the l -arginine–NO pathway in the rostral ventrolateral medulla is impaired in SHR and that this impairment may contribute to the increase in arterial pressure in this animal model of genetic hypertension.
Type of Medium:
Online Resource
ISSN:
0194-911X
,
1524-4563
DOI:
10.1161/01.HYP.31.4.1030
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
1998
detail.hit.zdb_id:
2094210-2
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